All chronic renal disorders eventually lead to renal interstitial fibrosis (RIF). Chronic inflammation and pro-fibrotic substances are familiar companions of the fibrotic process. The Sulforaphane (Sul) molecule is particularly useful in protecting the liver from oxidative damage. To investigate the Sul effects on fibrosis markers and inflammatory proteins in the kidney of NRK52E cell line and rats and clarify the mechanism of TGF-β/Smad signaling pathway in a rat model of RIF were developed in the present study. Sul (50, 100, and 200 ng/ml) remarkably reduced the gene expressions of tumor necrosis factor (TNF-α), interleukin-6 (IL-6), interleukin (IL)-1β, collagen 3 (COL3A1), collagen 1 (COL1A1), and α-smooth muscle actin (α-SMA) in fibrotic NRK52E cells compared with those in cells inspired by transforming growth factor-α (TGF-α). Histopathological investigations showed that Sul administration retained renal tissue structure and decreased kidney tissue fibrosis in rats subjected to unilateral ureteral blockage (UUO). The expression level of TNF-α, IL-6, IL-1β, COL3A1, COL1A1, and α-SMA in the rats’ kidneys exposed to UUO was also suppressed by the treatment of Sul. In the present study, western blot analysis showed that Sul upregulated the expressions of fibrotic NRK52E cells Smad7 and rat model UUO groups while simultaneously decreasing the stimulation of Smad2/3 and the expressions of cyclooxygenase-2, NF-κB, Smad4, activator protein-1, and high-mobility group protein B1. Ultimately, Sul’s ability to inhibit the TGF-β/Smad pathway and the development of inflammation factors may mitigate RIF.

中文翻译：

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萝卜硫素 (Sul) 通过控制炎症和 TGF-β/Smad 信号通路来减少肾间质纤维化 (RIF)

所有慢性肾脏疾病最终都会导致肾间质纤维化（RIF）。慢性炎症和促纤维化物质是纤维化过程中常见的伴随物。萝卜硫素 (Sul) 分子对于保护肝脏免受氧化损伤特别有用。为了探讨Sul对NRK52E细胞系和大鼠肾脏纤维化标志物和炎症蛋白的影响，并阐明TGF-β/Smad信号通路在RIF大鼠模型中的作用机制，本研究建立了RIF大鼠模型。Sul（50、100 和 200 ng/ml）显着降低肿瘤坏死因子 (TNF-α)、白细胞介素 6 (IL-6)、白细胞介素 (IL)-1β、胶原蛋白 3 (COL3A1)、胶原蛋白的基因表达纤维化 NRK52E 细胞中的 1 (COL1A1) 和 α-平滑肌肌动蛋白 (α-SMA) 与受转化生长因子-α (TGF-α) 启发的细胞中的细胞相比。组织病理学研究表明，在单侧输尿管阻塞 (UUO) 大鼠中，Sul 给药保留了肾组织结构并减少了肾组织纤维化。Sul处理也抑制了暴露于UUO的大鼠肾脏中TNF-α、IL-6、IL-1β、COL3A1、COL1A1和α-SMA的表达水平。在本研究中，蛋白质印迹分析表明，Sul上调纤维化NRK52E细胞Smad7和大鼠模型UUO组的表达，同时降低Smad2/3的刺激以及环氧合酶-2、NF-κB、Smad4、激活蛋白的表达- 1、高迁移率族蛋白B1。最终，Sul 抑制 TGF-β/Smad 通路和炎症因子发展的能力可能会减轻 RIF。